Fas (also known as Apo1 and CD95) is a cell surface receptor involved in apoptotic cell death. Fas expression and function were analyzed in three children (including two siblings) with a lymphoproliferative syndrome, two of whom also had autoimmune disorders. A large deletion in the gene encoding Fas and no detectable cell surface expression characterized the most affected patient. Clinical manifestations in the two related patients were less severe: Fas-mediated apoptosis was impaired and a deletion within the intracytoplasmic domain was detected. These findings illustrate the crucial regulatory role of Fas and may provide a molecular basis for some autoimmune diseases in humans.

Mutations inFasAssociated withHuman Lymphoproliferative Syndrome and Autoimmunity

Several theories claim that dreaming is a random by-product of REM sleep physiology and that it does not serve any natural function. Phenomenal dream content, however, is not as disorganized as such views imply. The form and content of dreams is not random but organized and selective: during dreaming, the brain constructs a complex model of the world in which certain types of elements, when compared to waking life, are underrepresented whereas others are over represented. Furthermore, dream content is consistently and powerfully modulated by certain types of waking experiences. On the basis of this evidence, I put forward the hypothesis that the biological function of dreaming is to simulate threatening events, and to rehearse threat perception and threat avoidance. To evaluate this hypothesis, we need to consider the original evolutionary context of dreaming and the possible traces it has left in the dream content of the present human population. In the ancestral environment human life was short and full of threats. Any behavioral advantage in dealing with highly dangerous events would have increased the probability of reproductive success. A dream-production mechanism that tends to select threatening waking events and simulate them over and over again in various combinations would have been valuable for the development and maintenance of threat-avoidance skills. Empirical evidence from normative dream content, children's dreams, recurrent dreams, nightmares, post traumatic dreams, and the dreams of hunter-gatherers indicates that our dream-production mechanisms are in fact specialized in the simulation of threatening events, and thus provides support to the threat simulation hypothesis of the function of dreaming.

https://www.unil.ch/files/live/sites/ln/files/shared/Revonsuo_1.pdf

The reinterpretation of dreams: An evolutionary hypothesis of the function of dreaming

During much of sleep, cortical neurons undergo near-synchronous slow oscillation cycles in membrane potential, which give rise to the largest spontaneous waves observed in the normal electroencephalogram (EEG). Slow oscillations underlie characteristic features of the sleep EEG, such as slow waves and spindles. Here we show that, in sleeping subjects, slow waves and spindles can be triggered noninvasively and reliably by transcranial magnetic stimulation (TMS). With appropriate stimulation parameters, each TMS pulse at <1 Hz evokes an individual, high-amplitude slow wave that originates under the coil and spreads over the cortex. TMS triggering of slow waves reveals intrinsic bistability in thalamocortical networks during non-rapid eye movement sleep. Moreover, evoked slow waves lead to a deepening of sleep and to an increase in EEG slow-wave activity (0.5-4.5 Hz), which is thought to play a role in brain restoration and memory consolidation.

http://www.tmslab.org/tms%20articles%20research/006.pdf

Triggering sleep slow waves by transcranial magnetic stimulation

A differential brain response to the subject's own name persists during sleep.

The process of falling asleep

Endogenous components of event-related potential appearing during NREM stage 1 and REM sleep in man

Electrophysiological evidence suggesting that sensory stimuli of unknown origin induce spontaneous K-complexes

Clinical characteristics of hepatitis C virus-associated retinopathy.

A case of recurrent unilateral varicella-zoster virus (VZV) retinitis is reported. The retinitis was characterized by arteriolitis and retinal necrosis with secondary chorioretinal atrophy localized in the periphery of the supratemporal quadrant of the retina. Polymerase chain reaction analysis of aqueous humor demonstrated VZV DNA in both the initial and recurrent episode. The Goldmann-Witmer coefficient for VZV IgG was elevated. The initial VZV retinitis was successfully treated with acyclovir and corticosteroids. Three years later, high-dose corti-costeroids alone were used to treat idiopathic facial nerve palsy. One month after concluding corticosteroids therapy, the VZV retinitis recurred in the same eye, suggesting that administration of the high-dose corticosteroids caused VZV reactivation and induced recurrence of VZV retinitis.

Naoki Satoh

Papers

Endogenous components of event-related potential appearing during NREM stage 1 and REM sleep in man

Electrophysiological evidence suggesting that sensory stimuli of unknown origin induce spontaneous K-complexes

Clinical characteristics of hepatitis C virus-associated retinopathy.

Recurrent varicella-zoster virus retinitis in a patient treated with systemic corticosteroids.

Suppression of Experimental Autoimmune Uveoretinitis by Dietary Calorie Restriction